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@Article{Zhang2015,
  author    = {Qiu-Yan Zhang and Hao Liang and Hou-Wu Gong and Hui-yong Huang and Xiao-qing Zhou and Xiang Sun},
  journal   = {Evidence-Based Complementary and Alternative Medicine},
  title     = {Correlations between Phlegm Syndrome of Chinese Medicine and Coronary Angiography: A Systematic Review and Meta-Analysis},
  volume    = {2015},
  year      = {2015},
  pages     = {1--12},
  doi       = {10.1155/2015/751743},
  publisher = {Hindawi Limited},
}

@Article{Zhang2020,
  author    = {Yonghui Zhang and Bing He and Haijiao Wang and Jianwei Shi and Hao Liang},
  issue     = {1},
  journal   = {Archives of Osteoporosis},
  title     = {Associations between bone mineral density and coronary artery disease: a meta-analysis of cross-sectional studies},
  volume    = {15},
  year      = {2020},
  month     = {feb},
  doi       = {10.1007/s11657-020-0691-1},
  publisher = {Springer Science and Business Media {LLC}},
}

@Article{Yang2020,
  author             = {Yang, Cheng-Long and Zeng, Yi-Di and Hu, Zhi-Xi and Liang, Hao},
  issue              = {2},
  journal            = {General physiology and biophysics},
  title              = {PCSK9 promotes the secretion of pro-inflammatory cytokines by macrophages to aggravate H/R-induced cardiomyocyte injury via activating NF- kB signalling.},
  volume             = {39},
  year               = {2020},
  month              = {Mar},
  pages              = {123-134},
  abstract           = {The upregulation of proprotein convertase subtilisin/kexin type 9 (PCSK9) was reported to be involved in regulating the levels of inflammatory markers and apoptosis in macrophages. This study aims to investigate the function and regulation of PCSK9 in myocardial ischaemia. The results of our study showed dramatically increased expression of PCSK9 induced by hypoxia/reoxygenation (H/R) stress rather than by apoptosis in primary murine cardiomyocytes and HL-1 cells. Moreover, PCSK9 promoted H/R-induced pro-inflammatory cytokine release from macrophages, while silencing of PCSK9 inhibited the expression of the pro-inflammatory cytokines TNF-α, IL-6 and IL-1β. Additionally, PCSK9 facilitated the release of pro-inflammatory cytokines from macrophages under H/R conditions, which decreased cardiomyocyte viability and promoted apoptosis of cardiomyocytes. For the underlying mechanisms, we identified PCSK9-induced NF-κB activation as being involved in the cardiomyocyte apoptosis, which was blocked by the NF-κB inhibitor BAY 11-7082. Collectively, this study provides new insights into the therapeutic possibility of regulating PCSK9 in cardiomyocytes for the treatment of ischaemic cardiomyopathy.},
  address            = {Slovakia},
  article-doi        = {10.4149/gpb-2019057},
  completed          = {20200903},
  history            = {2020/09/04 06:00 [medline]},
  keywords           = {Animals, Apoptosis, Cell Hypoxia, Cell Line, Cytokines/*metabolism, Gene Silencing, Macrophages/*cytology, Mice, Myocytes, Cardiac/*cytology, NF-kappa B/*metabolism, Proprotein Convertase 9/genetics/*metabolism, Signal Transduction},
  language           = {eng},
  linking-issn       = {0231-5882},
  location-id        = {10.4149/gpb-2019057 [doi]},
  nlm-unique-id      = {8400604},
  owner              = {NLM},
  print-issn         = {0231-5882},
  publication-status = {ppublish},
  registry-number    = {EC 3.4.21.- (Proprotein Convertase 9)},
  revised            = {20200903},
  source             = {Gen Physiol Biophys. 2020 Mar;39(2):123-134. doi: 10.4149/gpb-2019057.},
  status             = {MEDLINE},
  subset             = {IM},
  title-abbreviation = {Gen Physiol Biophys},
}

@Comment{jabref-meta: databaseType:bibtex;}
